Their results suggested that the STAT3, ERK1/2, and p38 MAPK pathways were involved in the production of IL-22-induced S100A8/A9 in FLSs, and were activated to stimulate the proliferation of FLSs and the production of monocyte chemoattractant protein 1 (MCP-1), further intensifying the process of inflammation in RA patients [48]. Here, S100A8 is linked to rheumatoid arthritis.